Engineering Transactions, 64, 4, pp. 533–540, 2016

Osteophyte Development During Osteoarthritis (OA) – Consideration of Angiogenesis, Mechanical Loading and Tissue Microstructure

Warsaw University of Technology

Warsaw University of Technology

This paper is devoted to modelling and investigation of the effects of mechanical loading, blood vessels development and tissue microstructure in osteoarthritis (OA) – a degenerative joint disease . OA is one of the most common diseases affecting the population, and therefore it is a social and medical problem of utmost importance. It predominantly affects the elderly but also sportsmen, obese people and those with curvature of the spine. Although the phenomenon of OA is not yet fully understood, it is commonly accepted that mechanical aspects are crucial in its evolution [1, 2]. Mechanical overloading leads to apoptosis of chondrocytes, which increases the generation of vascular endothelial growth factors [3]. A properly formulated mathematical model of cartilage degeneration and osteophytes development can significantly help in understanding the complexity of this process. The presented model reflects the most important aspects of the interactions between mechanical and biological factors, crucial for the phenomenon of OA.
and osteophytes development can significantly help to comprehend complexity of this
process. Presented model reflects the most important aspects of the interaction between
mechanical and biological factors crucial for osteoarthritis phenomenon.
Keywords: osteoarthritis; osteophyte; angiogenesis; mechanical loading; mathematical modelling; bone; cartilage
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Felson D.T., Osteoarthritis as disease of mechanics, Osteoarthritis and Cartilage, 21(1): 10–15, 2013, doi: 10.1016/j.joca.2012.09.012.

Wang T.-M. et al., Loading rates during walking in adolescents with Type II osteonecrosis secondary to pelvic osteotomy, Journal of Orthopedic Research, 2016, doi: 10.1002/jor.23239.

D’Lima D.D. et al., Human chondrocyte apoptosis in response to mechanical injury, Osteoarthritis and Cartilage, 9(8): 712–719, 2001. DOI: 10.1053/joca.2001.0468.

Pfander, D. et al., Vascular endothelial growth factor in articular cartilage of healthy and osteoarthritic human knee joints, Annals of Rheumatic Diseases, 60(11): 1070–1073, 2001, doi: 10.1136/ard.60.11.1070.

Pufe T. et al., Mechanical overload induces VEGF in cartilage discs via hypoxia-inducible factor, The American Journal of Pathology, 164(1): 185–192, 2004, doi: 10.1016/S0002-9440(10)63109-4.

Monod J., The growth of bacterial cultures, Annual Review of Microbiology, 3: 371–394, 1949, doi: 10.1146/annurev.mi.03.100149.002103.

Verhulst P.F., Deuxième memoire sur la loi ďaccrossement de la population, Mémoires de l'Académie Royale des Sciences, Des Lettres et des Beaux-Arts de Belgique, 20: 1–32, 1847.

Lekszycki T., dell’Isola F., A mixture model with evolving mass densities for describing synthesis and resorption phenomena in bones reconstructed with bio-resorbable materials, ZAMM (Journal of Applied Mathematics and Mechanics / Zeitschrift für Angewandte Mathematik und Mechanik), 92(6): 426–444, 2012, doi: 10.1002/zamm.201100082.

COMSOL Multiphysics ® v. 5.2, COMSOL AB, Stockholm, Sweden.

Hashimot S. et al., Development and regulation of osteophyte formation during experimental osteoarthritis, Osteoarthritis and Cartilage, 10(3): 180-187, 2002, doi: 10.1053/joca.2001.0505.

Kamekura S. et al., Osteoarthritis development in novel experimental mouse models induced by knee joint instability, Osteoarthritis and Cartilage, 13(7): 632–641, 2005, doi: 10.1016/j.joca.2005.03.004.

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